Glomerular size and the association of focal glomerulosclerosis in long-surviving human renal allografts.

Abstract

This biopsy study exploits the unique opportunity offered by long-surviving human renal allografts to analyze the effects of nephronopenia-induced glomerular hypertrophy on the association of focal glomerulosclerosis. Methods include glomerular morphometry and analysis of variance. Only allografts with focal glomerulosclerosis detected after 3 yr posttransplantation (Group TxFGS > 2 yr) have a group mean glomerular diameter (203.1 microns +/- SE (mean) 10.36) significantly larger (P < 0.05) than that of allografts biopsied beyond 2 yr posttransplantation but without focal glomerulosclerosis (Group No TxFGS > 2 yr; 158.3 microns +/- SE (mean) 8.32), allografts biopsied within 2 yr of transplantation with (Group TxFGS < 2 yr; 165.3 microns +/- SE (mean) 5.35) or without (Group NoTxFGS < 2 yr; 155.8 microns +/- SE (mean) 5.53) focal glomerulosclerosis, or allograft diameters at transplantation (Group CTx; 148.3 microns +/- SE (mean) 5.66). However, the increase is approximately 37% over that at transplantation, significantly less than the increase of approximately 70% attained by congenitally nephronopenic native kidneys (P < 0.50) with focal glomerulosclerosis (Group CNP; 264.4 microns +/- SE (mean) 11.01) over their controls (Group CN; 154.8 microns +/- SE (mean) 4.46). This observation suggests that the nephronopenic allograft has a curtailed ability for glomerular hypertrophy when compared with congenitally nephronopenic native kidneys and may explain the association of focal glomerulosclerosis in long-surviving renal homografts at a significantly smaller glomerular diameter. Although smaller, this appears to be the maximal glomerular dimension attained by long-surviving nephronopenic homografts in the absence of intrinsic glomerular disease (excluding focal glomerulosclerosis). Thus, these results are in accord with and offer further support for the general hypothesis that focal glomerulosclerosis develops in maximally hypertrophied glomeruli.